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STATE-OF-THE-ART PAPER

The Pathologic Continuum of Diabetic Vascular Disease

Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts

Manuscript received September 15, 2008; accepted September 30, 2008.

^_* Reprint requests and correspondence: Dr. Jorge Plutzky, Brigham and Women's Hospital, 77 Louis Pasteur Avenue, NRB 742, Boston, Massachusetts 02115 (Email: jplutzky{at}rics.bwh.harvard.edu).

Hyperglycemia can promote vascular complications by multiple mechanisms, with formation of advanced glycation end products and increased oxidative stress proposed to contribute to both macrovascular and microvascular complications. Many of the earliest pathologic responses to hyperglycemia are manifest in the vascular cells that directly encounter elevated blood glucose levels. In the macrovasculature, these include endothelial cells and vascular smooth muscle cells. In the microvasculature, these include endothelial cells, pericytes (in retinopathy), and podocytes (in renal disease). Additionally, neovascularization arising from the vasa vasorum may promote atherosclerotic plaque progression and contribute to plaque rupture, thereby interconnecting macroangiopathy and microangiopathy.

Key Words: glucose • atherosclerosis • advanced glycation end products • oxidative stress • inflammation

Abbreviations and Acronyms   AGE = advanced glycation end product   APC = activated protein C   CV = cardiovascular   EC = endothelial cell   ER = endoplasmic reticulum   PEDF = pigment epithelium-derived factor   PPAR = peroxisome proliferator-activated receptor   T2DM = type 2 diabetes mellitus   VEGF = vascular endothelial growth factor   VSMC = vascular smooth muscle cell

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